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The below mentioned article provides a short note on Gout.
Sodium urate crystals are precipitated out of solution and deposited in soft tissues, particularly in or about joints. These urate deposits are referred to as tophi. Acute inflammatory reactions called acute gouty arthritis is caused by the accumulation of sodium urate crystals in the tissues. The deposition of sodium urate tophi can cause chronic gouty arthritis which results in joint destruction.
Primary gout is an arthritis characterized by a derangement of purine metabolism, occurring mostly in males, with the elevation of serum uric acid concentration. The hyperuricemia of primary gout is due to excessive production of purines and to renal retention of uric acid. Excessive purine synthesis has been found to be due to deficiency of hypoxanthine guanine phosphoribosyl transferase.
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Decreased excretion of uric acid is due to a defect in the tubular secretory mechanism or the production of a metabolic inhibitor of this mechanism. The renal circulatory disturbances also cause defective excretion of uric acid. Hyperuricemia is a factor associated with an increased tendency to myocardial infarction.
In acute attacks of gout, serum uric acid concentration is as high as 10 mg and occasionally 15 mg/100 ml. The increased concentration of urate in the body fluids is the direct cause of the local tissue deposits in chronic goul.
Urates precipitate from the tissue fluids, because of their low solubility at the usual pH of the tissues and are deposited particularly in the kidneys, skin, subcutaneous tissues, cartilage, tendons, ligaments and synovial membranes. Acting as foreign bodies, these deposits incite an inflammatory reaction.
The ‘urate pool’, i.e., the amount of urate capable of mixing promptly with intravenously injected urate, is increased in subject with gout. ‘Secondary gout’ is applied to a condition with similar clinical signs with various disorders accompanied occasionally by elevation of serum uric acids. The secondary gout is accompanied by an increased rate of metabolic turnover of nucleic acids.
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Treatment of Gout:
1. Bed rest and colchicine for the acute attack.
2. Low purine diet.
3. Salicylates and/or small doses of colchicine for the inter-critical period.
4. Recently, the drug I has been discovered. This is an effective drug which can reduce the synthesis of uric acid.
It is the inhibitor of Xanthine oxidase. It can produce renal damage showing toxic effects.
5. Endomethacin, Phenylbutazone can be used as alternative drugs. These drugs do not cause abdominal cramp, vomiting and diarrhoea. But these drugs are not tolerated by peptic ulcer cases.
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6. Probenacid or Binemid can be given in dosage of 0.5 to 2.0 gm. daily combined with or without colchicine for reducing uric acid. It rarely causes nephrotic syndrome.
In the early stage of the disease, the patient should avoid foods of high purine content (meat, fish, beans, peas, sweet breads, liver and kidney) but he should take diets of low purine content (fruits, milk, cheese, eggs, sugar, sweets, vegetables). The patient should be advised to avoid alcohol and reduce weight for obesity. Surgery may be required to remove tophi.
